Panax

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Anil Kumar - One of the best experts on this subject based on the ideXlab platform.

  • gaba bzd receptor modulating mechanism of Panax quinquefolius against 72 h sleep deprivation induced anxiety like behavior possible roles of oxidative stress mitochondrial dysfunction and neuroinflammation
    Frontiers in Neuroscience, 2016
    Co-Authors: Priyanka Chanana, Anil Kumar
    Abstract:

    ABSTRACT Rationale- Panax quinquefolius (American Ginseng) is known for its therapeutic potential against various neurological disorders, but its plausible mechanism of action still remains undeciphered. GABA (Gamma Amino Butyric Acid) plays an important role in sleep wake cycle homeostasis. Thus there exists rationale in exploring the GABA-ergic potential of Panax quinquefolius as neuroprotective strategy in sleep deprivation induced secondary neurological problems. Objective- The present study was designed to explore the possible GABA-ergic mechanism in the neuro-protective effect of Panax quinquefolius against 72-hours sleep deprivation induced anxiety like behaviour, oxidative stress, mitochondrial dysfunction, HPA-axis activation and neuroinflammation. Materials and Methods- Male laca mice were sleep deprived for 72-hours by using Grid suspended over water method. Panax quinquefolius (American Ginseng 50, 100 and 200 mg/kg) was administered alone and in combination with GABA modulators (GABA Cl- channel inhibitor, GABA-benzodiazepine receptor inhibitor and GABAA agonist) for 8 days, starting five days prior to 72-hours sleep deprivation period. Various behavioural (locomotor activity, mirror chamber test), biochemical (lipid peroxidation, reduced glutathione, catalase, nitrite levels), mitochondrial complexes, neuroinflammation marker (Tumour Necrosis Factor, TNF-alpha), serum corticosterone, and histopathological sections of brains were assessed. Results- 72-hours sleep deprivation significantly impaired locomotor activity, caused anxiety-like behaviour, conditions of oxidative stress, alterations in mitochondrial enzyme complex activities, raised serum corticosterone levels, brain TNFα levels and led to neuroinflammation like signs in discrete brain areas as compared to naive group. Panax quinquefolius (100 and 200 mg/kg) treatment restored the behavioural, biochemical, mitochondrial, molecular and histopathological alterations. Pre-treatment of GABA Cl- channel inhibitor as well as GABA-benzodiazepine receptor inhibitor, significantly reversed the protective effect of P. quinquefolius (100 mg/kg) in 72-hours sleep deprived animals (P<0.05). However, pretreatment with GABAA agonist, potentiated Panax quinquefolius’s protective effect which was significant as compared to their effect per se (p<0.05). Conclusion- GABA-ergic mechanism could be involved in the neuroprotective effect of P. quinquefolius against sleep deprivation induced anxiety-like behaviour, oxidative stress, mitochondrial dysfunction, HPA axis activation and neuroinflammation.

Leeyan Sheen - One of the best experts on this subject based on the ideXlab platform.

Liu Diqiu - One of the best experts on this subject based on the ideXlab platform.

  • Oleanane-Type Saponins Biosynthesis in Panax notoginseng via Transformation of β-Amyrin Synthase Gene from Panax japonicus.
    Journal of agricultural and food chemistry, 2019
    Co-Authors: Xiang Zhang, Jiang Sen, Xiang Yingying, Liu Diqiu
    Abstract:

    Oleanane-type saponins considered as the main medicinal ingredients in Panax japonicus are not found in Panax notoginseng. β-Amyrin synthase (βAS) was recognized as the first key enzyme in the biosynthetic branch of oleanane-type saponins. In this study, βAS gene from P. japonicus (PjβAS) was transferred into P. notoginseng cells. Along with PjβAS expression in the transgenic cells, the expression levels of several key enzyme genes related to triterpenoid saponins biosynthesis and the content of P. notoginseng saponins were also increased. Two oleanane-type saponins, chikusetsusaponin IV and chikusetsusaponin IVa, contained in P. japonicus were first discovered in transgenic P. notoginseng cells. This study successfully constructed a biosynthetic pathway of oleanane-type saponins in P. notoginseng by introducing just one gene into the species. On the basis of this discovery and previous studies, the common biosynthetic pathway of triterpenoid saponins in Panax genus may be unified to some extent.

Jane C J Chao - One of the best experts on this subject based on the ideXlab platform.

  • ginseng extract and ginsenoside rb1 attenuate carbon tetrachloride induced liver fibrosis in rats
    BMC Complementary and Alternative Medicine, 2014
    Co-Authors: Ya Hui Tsai, Jane C J Chao
    Abstract:

    Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl4)-induced hepatitis and liver fibrosis in rats. Male Sprague–Dawley rats were randomly divided into four groups: control, CCl4, CCl4 + 0.5 g/kg Panax ginseng extract and CCl4 + 0.05 g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9 weeks. Liver injury was induced by intraperitoneally injected with 400 ml/l CCl4 at a dose of 0.75 ml/kg body weight weekly for 7 weeks. The control group was intraperitoneally injected with olive oil. The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1β (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05). Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl4-induced liver fibrosis through down-regulation of hepatic prostaglandin E2 and TIMP-1.

Priyanka Chanana - One of the best experts on this subject based on the ideXlab platform.

  • gaba bzd receptor modulating mechanism of Panax quinquefolius against 72 h sleep deprivation induced anxiety like behavior possible roles of oxidative stress mitochondrial dysfunction and neuroinflammation
    Frontiers in Neuroscience, 2016
    Co-Authors: Priyanka Chanana, Anil Kumar
    Abstract:

    ABSTRACT Rationale- Panax quinquefolius (American Ginseng) is known for its therapeutic potential against various neurological disorders, but its plausible mechanism of action still remains undeciphered. GABA (Gamma Amino Butyric Acid) plays an important role in sleep wake cycle homeostasis. Thus there exists rationale in exploring the GABA-ergic potential of Panax quinquefolius as neuroprotective strategy in sleep deprivation induced secondary neurological problems. Objective- The present study was designed to explore the possible GABA-ergic mechanism in the neuro-protective effect of Panax quinquefolius against 72-hours sleep deprivation induced anxiety like behaviour, oxidative stress, mitochondrial dysfunction, HPA-axis activation and neuroinflammation. Materials and Methods- Male laca mice were sleep deprived for 72-hours by using Grid suspended over water method. Panax quinquefolius (American Ginseng 50, 100 and 200 mg/kg) was administered alone and in combination with GABA modulators (GABA Cl- channel inhibitor, GABA-benzodiazepine receptor inhibitor and GABAA agonist) for 8 days, starting five days prior to 72-hours sleep deprivation period. Various behavioural (locomotor activity, mirror chamber test), biochemical (lipid peroxidation, reduced glutathione, catalase, nitrite levels), mitochondrial complexes, neuroinflammation marker (Tumour Necrosis Factor, TNF-alpha), serum corticosterone, and histopathological sections of brains were assessed. Results- 72-hours sleep deprivation significantly impaired locomotor activity, caused anxiety-like behaviour, conditions of oxidative stress, alterations in mitochondrial enzyme complex activities, raised serum corticosterone levels, brain TNFα levels and led to neuroinflammation like signs in discrete brain areas as compared to naive group. Panax quinquefolius (100 and 200 mg/kg) treatment restored the behavioural, biochemical, mitochondrial, molecular and histopathological alterations. Pre-treatment of GABA Cl- channel inhibitor as well as GABA-benzodiazepine receptor inhibitor, significantly reversed the protective effect of P. quinquefolius (100 mg/kg) in 72-hours sleep deprived animals (P<0.05). However, pretreatment with GABAA agonist, potentiated Panax quinquefolius’s protective effect which was significant as compared to their effect per se (p<0.05). Conclusion- GABA-ergic mechanism could be involved in the neuroprotective effect of P. quinquefolius against sleep deprivation induced anxiety-like behaviour, oxidative stress, mitochondrial dysfunction, HPA axis activation and neuroinflammation.